Serum and urinary TGF-β
1 levels were determined by ELISA before and after L-arginine in, ion (LA), which inhibits tubular reabsorption o, roteins, in 49 NIDDM patients with, DDM-II, N=23) or without microalbuminuria (MAU), DDM-I, N=26) and in healthy controls (N=35) to elucidate the pathogenetic role of TGF-β
1 in the development of MAU. Serum or urinary TGF-β
1 was significantly correlated with FPG (r=0.22-0.49) and HbA1c (r=0.36-0.51). Serum TGF-β1 in the, NIDDM groups was sli, ly, in part significantly, higher than in the control group. LA increased urinar, GF-β1 in all groups, and that in NIDDM-II (0.46±0.06→1.30±, 0ng/hr) was the highest, and that in NIDDM-I (0.37±0.04→0.91±0.05ng/hr) was higher than in the controls (0.19±0.02→0.66±0.05ng/hr), n the group as a whole, urinary TGF-β
1 before and after LA was correlated with the AER (r=0.26 vs r=0.63) and glomerular filtr, on of albumin (r=0.36 vs r=0.59), and inversely correlated with the rate of tubular album, reabsorption (r=0.37 vs r=0.49), the stronger correlation being, nd after LA. On the other hand, serum TGF-β
1 was not significantly correlated with either of them (r=0.13-0.02). Thes, esults indicate that urinary TGF-β,
1, exaggeratedly produced by hyperglycemia, plays a permissive role in the development of MAU in NIDDM.
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